Schizophrenia Flashcards

1
Q

When does schizophrenia typically start?

A

Adolescence or as a young adult

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2
Q

What are examples of first rank symptoms?

A
  • Delusion
  • Auditory hallucination
  • Thought disorder e.g. thought withdrawal
  • Passivity phenomena e.g. ‘made’ feelings
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3
Q

What is a delusion?

A
  • Fixed rigidly held belief not understandable on the basis of a patient’s cultural background
  • Typically dominates thinking and is socially disabling
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4
Q

What are negative symptoms?

A
  • Persistent loss of usual activities and interests, apathy, blunted emotional responses, speech reduction
  • Social withdrawal, impaired attention, anhedonia, lethargy
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5
Q

What is passivity phenomena?

A
  • Patients belief that they no longer control their actions, feelings or thoughts
  • External agent controlling them to act, feel or think
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6
Q

What is presented in Whitford’s theory, which explains the symptoms of schizophrenia?

A

The concept of brain abnormalities and abnormal salience (hallucinations and delusions) and agency (passivity phenomena)

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7
Q

What does Whitford’s theory suggest as the cause of schizophrenia?

A
  • SZ arises because of some incompletely understood genetic trigger during late adolescence/early adulthood
  • Myelin is structurally abnormal and consequently abnormal in ability to insulate axon membranes affecting velocity of axon potentials
  • Functional disconnections result in disruption of corollary discharge mechanisms
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8
Q

What is the risk of SZ in monozygotic twins or a child with both parents having SZ?

A

45% increased risk of having SZ

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9
Q

What is the risk to children of SZ mothers adopted soon after birth by non-SZ families?

A

13% increased risk - no increased risk of developing SZ for children of non-SZ parents similarly adopted

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10
Q

What is the problem with molecular genetic studies in SZ?

A
  • They have not identified clinically useful findings for drug discovery nor does this seem likely
  • There are multiple genes implicated in SZ each with very little effect
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11
Q

Where are the biggest white matter abnormalities in the brains of SZ patients?

A

Corona radiata and corpus callosum

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12
Q

What is corollary discharge?

A
  • Efference copy of motor command is used to create a predicted sensory feedback (corollary discharge) which estimates the sensory consequences of a motor command
  • Actual sensory feedback compared with predicted feedback informs the CNS about external actions
  • This is how you know the difference between external world movement and self-generated eye movement
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13
Q

How does abnormal corollary discharge relate to auditory hallucinations in SZ patients?

A

Auditory hallucinations are due to a failure of corollary discharge connections due to impaired white matter tract integrity from Broca’s area to superior temporal gyrus/Wernicke’s area so auditory hallucinations are untagged sub-vocal speech therefore not recognised by the brain as self-generated

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14
Q

What is the altered sense of agency in SZ thought to be due to?

A

Dysfunction of perception and action therefore faulty integration of prior knowledge and expectations with evidence

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15
Q

What are the 2 separate cues to sense of agency?

A
  • Sensorimotor system and cognitive system
  • The widely held view currently - physiological prediction deficit in sensorimotor function leads to distorted agency cues
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16
Q

What are the 2 ways in which linkage of action and effect are generated?

A
  • Predicatively (action predicted to generate a given effect) - corollary discharge
  • Retrospectively (inference action caused effect) - cognitive mechanism
17
Q

In terms of predictive and retrospective components of intentional binding, what do SZ patients lack?

A
  • Absent predictive component with strong retrospective component
  • Higher incidence of first rank symptoms, such as delusions and hallucinations, associated with more reduced predictive component
18
Q

What is the key mechanism underlying the sense of agency?

A

Association between ones action and external effect

19
Q

What did the Moore et al (2012) review show about the prediction component of intentional binding?

A

Patients were generating imprecise prediction rather than no predictions

20
Q

Why could hyperdopaminergia occur in SZ?

A

If the brain’s response to constantly experiencing internally generated events as unexpected external events is to increase dopamine firing then hyperdopaminergia results

21
Q

The mesolimbic DA system is a critical component of the attribution of salience. Describe the process of salience

A

This is the process by which events and thought grab attention and influence goal-directed behaviour because of association with reward or punishment, linked to concepts of value

22
Q

How is salience related to delusions and auditory hallucinations?

A
  • Delusions - belief with extremely high abnormal salience
  • Auditory hallucinations - abnormally high salience of internal thoughts
23
Q

How does DA affect salience?

A

In health, DA mediates the process of salience acquisition and expression but does not create the process (DA release is dependent on external stimuli)

24
Q

What happens to DA release and thus salience in psychosis?

A
  • There is dysregulated DA transmission leading to stimulus independent release of DA
  • This leads to creation of abnormal saliences (psychotic symptoms)
25
What property do all anti-psychotics have in common?
They dampen salience acquisition
26
How was dampening of salience by anti-psychotics demonstrated in behavioural studies in rats in the 1950s?
* Rats had a punishment avoidance schedule - associated bell with an electric shock, so would try to avoid * Rats + anti-psychotics - function not impaired and still responding to shock but there is a forgetfulness of motive i.e. reduced salience
27
What pathways are punishment avoidance and reward-learning associated with respectively?
* Indirect basal ganglia pathway and D2 receptors * Reward learning is associated with direct basal ganglia pathway and D1 receptors
28
What property do anti-psychotics need to have to be clinically effective?
They need to block D2 receptors (indirect basal ganglia pathway)
29
Name some examples of typical anti-psychotics
Chlorpomazine, haloperidol
30
Name some examples of atypical anti-psychotics
Clozapine, olanzapine, risperidone, quetiapine
31
Why are regular blood counts needed for patients on clozapine?
Risk of agranulocytosis
32
What are some clinical factors of SZ associated with a good prognosis?
* Female, abrupt onset, married, good pre-morbid social adjustment, short duration of illness, **lack of negative symptoms, lack of cognitive impairment**, no ventricular enlargement * Bold = if present tend to indicate poor prognosis
33
10% of SZ patients commit suicide. What factors makes this more likely?
Early in illness, males with chronic illness, unemployed, tardive dyskinesia, previous high educational attainment, sudden stoppage of medication, recent discharge from hospital
34
Grey matter abnormalities occur early in SZ. Why are these abnormalities thought to occur?
* Due to neuropil elimination not neuronal death * Most likely loss of dendritic arbors and associated synaptic infrastructure
35
What areas of the brain have been shown to atrophy in SZ?
Smaller hippocampus, amygdala, thalamus, nucleus accumbens